Skeletal muscle assessment to understand cardiometabolic interactions
© Kumar et al. 2016
Published: 27 January 2016
Patients with diabetes and metabolic disorders have excess mortality after myocardial infarction (MI). Their mitochondrial function is often abnormal, and can be measured with phosphorus magnetic resonance spectroscopy (PMRS). Participation in a program of cardiac rehabilitation and secondary prevention (CRSP) reduces post-MI mortality, but typically involves only aerobic exercise and may not sufficiently improve mitochondrial function. An integrated assessment of skeletal muscle would potentially be useful to assess the impact of aerobic plus resistive exercise post-MI.
We tested a combined MR-based protocol with: 1) PMRS of quadriceps muscle at rest, during 30s of isometric quadriceps exercise, and during recovery and 2) quadriceps muscle fat quantification using a multi-echo Dixon sequence at 1.5 Tesla (Siemens, Erlangen). After shimming, an unlocalized FID sequence using the following parameters was used to acquire 31P spectra: TR = 1000 ms, TE = 0.34 ms, BW = 2000 Hz, points = 1024, averages = 4. Fat/water quantification was acquired with: TR = 11.1 ms, 6 echoes with TE minimized, BW = 1150 Hz, slice thickness = 4 mm.
PCr peak amplitudes, representing concentration, were quantified using jMRUI (Lyons, France) and recovery time was calculated with a best-fit mono-exponential function (Fig 1A). Quantitative fat maps were generated from the Dixon sequence, with pixel intensity representing fat percentage (Fig 1C). Feasibility was assessed in healthy volunteers and patients starting a CRSP program post-MI.
Nine volunteers and 15 patients were enrolled. Left ventricular ejection fraction was preserved in CRSP patients (56 ± 10%). Maximum exertion ability, measured before starting CRSP was similar in diabetic and non-diabetic patients (3.05 ± 0.6 vs. 3.4 ± 0.8 metabolic equivalents [METs], p = 0.4). Hba1c averaged 7.8% in diabetics whose LDL levels averaged 109.7 ± 51.5 vs. 106.7 ± 33.4 mg/dL in nondiabetics (p=0.9). PCr recovery time was longer (41.9 ± 1.4 vs. 32.1 ± 7.4 s, p = 0.05), and intramuscular fat percentage higher in CRSP patients vs. controls (8.7 ± 2.9 vs. 2.54 ± 0.6%, p < 0.001) (Fig 1B,D). Intramuscular fat percentage was similar in diabetic and non-diabetic patients prior to starting CRSP (p =0.4), and PCr recovery time tended to be longer in diabetic patients compared to nondiabetic patients and controls (p=0.03 for trends across groups). Preliminary follow-up data suggest considerably worse improvement in METs in diabetic vs. nondiabetic patients (delta = 1.0 ± 0.8 vs. 4.0 ± 2.4, p = 0.06).
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